The reason for this controversy stems from the fact that ACEIs and ARBs use may increase the expression of ACE2 receptor in animal-based studies,7,8 which is the known cellular receptor and a necessary entry point for SARS-COV-2 infection.9 Conversely, it has been indicated that ACE2 expression is downregulated following SARS infection, resulting in excessive activation of RAS and exacerbated pneumonia progression.10 Therefore, administration of ACEI/ARB may, in turn, be beneficial by blocking ACE2 downregulation-induced hyperactivation of RAS and thereby preventing acute lung injury. Here, ACE2 is linked to pneumonia.